Polysaccharides from Enteromorpha prolifera protect against carbon tetrachloride-induced acute liver injury in mice via activation of Nrf2/HO-1 signaling, and suppression of oxidative stress, inflammation and apoptosis. Issue 5 (7th May 2020)

• Record Type: Journal Article
• Authors: Guo, Fuchuan; Zhuang, Xinyun; Han, Mengyuan; Lin, Wenting
• Is Part Of: Food & function. Volume 11:Issue 5(2020)
• Page Start: 4485
• Page End: 4498
• Publication Date: 2020-05-07
• Subjects: Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; Nutrition -- Periodicals; 664.07
• DOI: 10.1039/d0fo00575d
• Languages: English
• ISSNs: 2042-6496

Abstract

Abstract : EPP protected against hepatic injury induced by CCl4 -derived reactive intermediates through the suppression of hepatic oxidative stress, inflammation, and apoptosis. Abstract : To investigate whether polysaccharides from Enteromorpha prolifera (EPP) could protect against acute hepatic injury induced by CCl4, ICR mice were pretreated with EPP (150, 300, and 450 mg kg −1 ) and silymarin (100 mg kg −1 ) for 28 days before CCl4 induction. Pretreatment with EPP attenuated CCl4 -induced elevated serum transaminase activities and histopathological alterations in the liver. In addition, EPP prevented CCl4 -induced reduction of protein levels of phosphorylated nuclear factor E2-related factor 2 (p-Nrf2)/Nrf2, heme oxygenase-1 (HO-1), and mRNA levels of NADPH quinineoxidoreductase-1 (NQO-1), which, in turn, reduced hepatic oxidative stress injury. Furthermore, the hepatic protein levels of inflammatory mediators and the phosphorylation of nuclear factor-kappaB p65 (NF-κB p65) and I kappaB alpha (IκBα), and the mRNA levels of Toll-like receptor 2 (TLR2), TLR4, and prolyl-isomerase-1 (Pin-1) in the inflammatory signaling pathway were recovered in the EPP pretreated groups. Moreover, EPP prevented the hepatocellular apoptotic changes with inhibition of B-cell lymphoma 2 (Bcl-2), and the induction of Bcl-2-associated X (Bax) and Cleaved caspase-3 caused by CCl4 . Taken together, these results indicated that EPP protected against hepatic injury induced by CCl4 -derived reactive intermediates through the activation of Nrf2/HO-1 signaling, and suppression of oxidative stress, inflammation and apoptosis.